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No differences were noted between the two groups with respect to secondary outcome measures, including time to endpoint, occurrence of fever, type and number of microbiologically documented infections, and administration of intravenous antibiotics.
They found that tumor progression of the experimental group is 10.77 times slower than that of the control group which receives no intervention, and the median time to endpoint for the experimental group (49 days) is 32.4% longer than that for the control group (37 days), which indicates that the intervention is quite efficient.
However, we did find sex differences on time to endpoint on the hybrid C57BL/6J-BALB/c strain.
Neither the study of Heiman-Patterson and colleagues (Heiman-Patterson, 2005), nor our study here found sex differences in time to endpoint on the C57BL/6J background.
The FVB background showed the shortest mean average time to endpoint, followed by BALB/c, C3H, hybrid B6-BALB/c and finally the B6 background, which presented the longest survival time (Fig. 1B, Table 1).
Subjects were followed for ~24 months, with the primary outcome of time to "endpoint," defined as the development of symptoms severe enough to require treatment with levodopa, as determined by a blinded clinician.
Similar(50)
Interim additions had predictably longer times to endpoint.
The association of various factors with the hazards of failure for the time-to-endpoint PFS was estimated using the Cox proportional hazard regression model.
Tumour quadrupling or tripling times were chosen as time-to-endpoint (TTE), which were determined by using the nonlinear regression analysis for exponential growth of each individual tumour growth data set from each experimental animal.
Times to endpoints from onset of progression showed trends for the interval but were no longer significant.
For example, only baseline viral load, CD4+ cell count, and study were predictive of both the time to TRDF endpoint and the purely virologic time to ERDF endpoint.
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